Uric acid is a naturally occurring metabolite of a number of typically ingested compounds, especially xanthines such theobroma (in chocolate), caffeine, etc, and is generally disposed of by the body by execretion into the urine from the blood. When uric acid production is high or its elimination from the body is low so that serum levels are at high levels for considerable periods of time, there is the risk that uric acid crystals will begin to form at various points in the body. When these crystals become large enough to become painful, clinical conditions such as gout, gouty arthritis, and uric acid stones (urinary and elsewhere) result. Such situations may result from disease states or may be drug induced, for example, serum uric acid levels are elevated with a substantial number of diuretic drugs, most notably the thiazide diuretics, and upon cytotoxic antineoplastic agent administration and cyclosporin A. Clinical conditions associated with elevated serum uric acid include gout, gouty arthritis, gouty nephropathy, eclampsia, and diseases that involve accelerated formation and destruction of blood cells.
Upon diagnosis of the elevated serum uric acid, therapies which are begun have included dietary intervention (to reduce intake of substances which are metabolized to uric acid), intervention in the metabolic pathways leading to uric acid (i.e. allopurinol which inhibits xanthine oxidase from converting hypoxanthine and xanthine to uric acid) and uricosurics such as probenecid or sulfinpyrazone, which increase the amount of uric acid resulting in the urine by improving its passage into the urine from the blood or by interfering in its reuptake.
Overwhelmingly, in recent times the mainstay of treatment for excess uric acid conditions has been the use of allopurinol. The typical uricosurics have required doses of large amounts [cite probenecid dosage] so as to make compliance difficult. In addition, large volumes of fluids have been necessary for both maintaining the urine concentration of uric acid low enough and to permit the uricosuric to sufficiently pass through the system. In addition standard uricosurics have their own problems associated therewith. For example, sulfinpyrazone should not really be given to patients with a history of peptic ulcer disease, phenylbutazone has this same problem as well as severe blood dyscrasias associated with its use such that it is not used for chronic administration, probenecid should be administered to patients with history of peptic ulcer disease only with caution; anticoagulents such as coumarins and indandiones and oral hypoglycemics of the sulfonylurea group, while having some uricosuric property are unsuited to being used for their uricosuric property generally due to their primary activities.